NDT Advance Access originally published online on February 22, 2005
Nephrology Dialysis Transplantation 2005 20(4):673-677; doi:10.1093/ndt/gfh734
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© The Author [2005]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org
Editorial Comment
Do not be misguided by guidelines: the calcium x phosphate product can be a Trojan horse
1 Department of Nephrology and Clinical Immunology and 2 IZKF BioMAT, University Hospital Aachen, Germany
Correspondence and offprint requests to: PD Dr Med. Markus Ketteler, Medizinische Klinik II: Nephrologie und Klinische Immunologie, Universitätsklinikum Aachen, Pauwelsstr. 30, D-52057 Aachen, Germany. Email: mketteler@ukaachen.de
Keywords: calcium; cardiovascular mortality; dialysis; fetuin; hyperphosphataemia; hyperparathyroidism; phosphate; PTH
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Introduction |
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In recent years, it has become increasingly evident that the dramatic cardiovascular mortality of end-stage renal disease (ESRD) patients is connected with disturbances in calcium and phosphate homeostasis. While for decades the manifestations of secondary and tertiary hyperparathyroidism were largely regarded as particular forms of bone disease, it is now common sense that extraosseous and especially cardiovascular calcifications may develop as a consequence of an increased extracellular availability of calcium and phosphate ions in this setting. This ‘paradigm shift’ with regard to renal osteodystrophy led to the publication of the K/DOQI guidelines in October 2003 which, in addition to defining target levels of intact parathyroid hormone (iPTH) in different stages of kidney failure, now recommend target levels for serum phosphate (P), serum calcium (Ca) and the Ca x P product [1]. While these guidelines represent a major step forward to improved cardiovascular prevention in ESRD patients, we wish
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Deranged Ca and P homeostasis as a cardiovascular risk factor |
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The one side of the coin
The other side of the coin
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Extraosseous calcification: why are we all ‘metastable’? |
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Lessons from uraemic calcification-prone mice |
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Is a high Ca x P product in serum always harmful? |
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Conclusion |
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